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accession-icon GSE12421
Analysis of OBF-1 overexpression in early B cells
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

OBF1, also known as Bob.1 or OCA-B, is a B lymphocyte-specific transcription factor which coactivates Oct1 and Oct2 on B cell specific promoters. So far, the function of OBF1 has been mainly identified in late stage B cell populations. The central defect of OBF1 deficient mice is a severely reduced immune response to T cell-dependent antigens and a lack of germinal center formation in the spleen. Relatively little is known about a potential function of OBF1 in developing B cells. Here we have generated transgenic mice overexpressing OBF1 in B cells under the control of the immunoglobulin heavy chain promoter and enhancer. Surprisingly, these mice have greatly reduced numbers of follicular B cells in the periphery and have a compromised immune response. Furthermore, B cell differentiation is impaired at an early stage in the bone marrow. A first block is observed during B cell commitment and a second differentiation block is seen at the large preB2 cell stage. The cells that succeed to escape the block and to differentiate into mature B cells have post-translationally downregulated the expression of transgene, indicating that expression of OBF1 beyond the normal level early in B cell development is deleterious. Indeed ID3, which is a negative regulator of B cell differentiation, is upregulated in the EPLM and preB cells of the transgenic mice. Furthermore ID3 promoter contains an octamer site suggesting that it is a potential OBF-1 direct target gene. These results provide evidence that OBF1 expression has to be tightly regulated in early B cells to allow efficient B lymphocyte differentiation.

Publication Title

Enforced expression of the transcriptional coactivator OBF1 impairs B cell differentiation at the earliest stage of development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE40197
Genome wide analysis of RNA species present in SMN-containing RNPs
  • organism-icon Mus musculus
  • sample-icon 5 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Several studies indicate that SMN-containing mRNP complexes could be involved in the axonal localization of a large number of mRNAs. We have used murine motor neuron-like NSC-34 cells and RNA Immuno-Precipitation experiments coupled to microarray analyses to perform a genome-wide analysis of RNA species present in mRNP complexes containing the full length SMN protein (flSMN). In situ hybridization and immuno-fluorescence experiments performed on several candidates indicate that these mRNAs colocalize with the SMN protein in neurites and axons of differentiated NSC-34 cells. Moreover, they localize in cell processes in a SMN-dependent manner. Thus, low SMN levels might result in localization deficiencies of mRNAs required for axonogenesis.

Publication Title

Genome-wide identification of mRNAs associated with the protein SMN whose depletion decreases their axonal localization.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE1462
Mitochondrial disorders
  • organism-icon Homo sapiens
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Genome U133A Array (hgu133a)

Description

Extremely variable clinic and genetic features characterize Mitochondrial Encephalomyopathy Disorders (MED). Pathogenic mitochondrial DNA (mtDNA) defects can be divided into large-scale rearrangements and single point mutations. Clinical manifestations become evident when a threshold percentage of the total mtDNA is mutated. In some MED, the "mutant load" in an affected tissue is directly related to the severity of the phenotype. However, the clinical phenotype is not simply a direct consequence of the relative abundance of mutated mtDNA. Other factors, such as nuclear background, can contribute to the disease process, resulting in a wide range of phenotypes caused by the same mutation. Using Affymetrix oligonucleotide cDNA microarrays (HG-U133A), we studied the gene expression profile of muscle tissue biopsies obtained from 12 MED patients (4 common 4977-bp deleted mtDNA and 8 A3243G: 4 PEO and 4 MELAS phenotypes) compared with age-matched healthy individuals.

Publication Title

Skeletal muscle gene expression profiling in mitochondrial disorders.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE7038
RLSC and MMH-D3 cell lines
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Increasing evidence provide support that the mammalian liver contains stem/progenitor cells, but their molecular phenotype, embryological derivation, cell biology as well as of their role in the liver cell turnover and regeneration remain to be further clarified.

Publication Title

Isolation and characterization of a murine resident liver stem cell.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE3075
Transplantation of ALDHhiSSClo Neural Stem Cells in nmd Mice, an Animal Model of SMARD1
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

SMARD1 is an infantile autosomal recessive motor neuron (MN) disease, caused by mutations in the Immunoglobulin mu binding protein 2 (IGHMBP2).

Publication Title

Transplanted ALDHhiSSClo neural stem cells generate motor neurons and delay disease progression of nmd mice, an animal model of SMARD1.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP135286
GPR68 senses flow and is essential for vascular physiology
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 1000

Description

GPR68 is an essential flow sensor in arteriolar endothelium, and is a critical signaling component in cardiovascular pathophysiology Overall design: RNAseq of cells from mesenteric endothelium of mice plus and minus GPR68

Publication Title

GPR68 Senses Flow and Is Essential for Vascular Physiology.

Sample Metadata Fields

Specimen part, Cell line, Treatment, Subject

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accession-icon GSE6540
Expression data from olfactory epithelium of Lip-C-treated mice compared to Lip-O-treated control mice
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Microarray analysis of gene expression in the olfactory epithelium of macrophage depleted mice to study the role of macrophages in regulating neurodegeneration, neuroprotection, and neurogenesis of olfactory sensory neurons

Publication Title

Macrophage-mediated neuroprotection and neurogenesis in the olfactory epithelium.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE50698
DENV1-NS3hell single point mutations enhance viral replication and bypass Type I IFN anti-virus function in human dendritic cells
  • organism-icon Homo sapiens
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Human Gene 1.0 ST Array (hugene10st)

Description

Dengue is one of the most important arboviruses in the world, with 2.5 billion people living in areas under risk to contagious. Mosquitos from Aedes genus is the transmission vector of viral particles.

Publication Title

Single point mutations in the helicase domain of the NS3 protein enhance dengue virus replicative capacity in human monocyte-derived dendritic cells and circumvent the type I interferon response.

Sample Metadata Fields

Specimen part, Time

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accession-icon GSE10224
Gene Expression Analysis of laser-microdissected motorneurons in Spinal Muscular Atrophy (SMA)
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Expression 430A Array (moe430a)

Description

Spinal Muscular Atrophy (SMA) is an autosomal recessive motor neuron disease and is the second most common genetic disorder leading to death in childhood. Stem cell transplantation could represent a therapeutic approach for motor neuron diseases such as SMA. We examined the theraputics effects of a spinal cord neural stem cell population and their ability to modify SMA phenotype.

Publication Title

Neural stem cell transplantation can ameliorate the phenotype of a mouse model of spinal muscular atrophy.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE15071
Detection of genomic deletions in rice by genomic DNA hybridization to oligonucleotide microarrays
  • organism-icon Oryza sativa indica group
  • sample-icon 17 Downloadable Samples
  • Technology Badge Icon Affymetrix Rice Genome Array (rice)

Description

Rice deletion mutants have not been widely used in functional genomics, because the mutated genes are not tagged and therefore, difficult to identify

Publication Title

Detection of genomic deletions in rice using oligonucleotide microarrays.

Sample Metadata Fields

Specimen part

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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